Vinblastine (U.S. Pat. No. 3,097,137) has been employed for a number of years as an oncolytic agent particularly useful in the treatment of Hodgkin's Disease and other lymphomas. It is generally administered by the intravenous route to patients suffering from one of these diseases. There has been a sparse amount of research work reported involving vinblastine, or other oncolytic vinca alkaloids and their derivatives, directed toward their physiological action in non-neoplastic conditions. For example, vinblastine has been used to induce leucopenia in experimental animals and the effect of that leucopenia on other conditions studied. Phelps and McCarty, writing in J. Exp. Med., 124 115 (1966), induced a gouty arthritis type of inflammation in dogs by the injection into the joint of microcrystalline sodium urate. An acute inflammatory reaction was ordinarily produced, but, in dogs pretreated with vinblastine at such a dose level that there was a profound leukocyte depletion, significant phagocyte accumulation was prevented and the inflammatory response was almost completely abolished. This finding led the authors to the conclusion that, in the particular experimental model, the polymorphonuclealeukocyte was necessary to the urate-crystal induced inflammation. Chang and Gralla, writing in Arthritis and Rheumatism, 11, 145 (1968), investigated the possibility that the effects of vinblastine on joint inflammation found by Phelps and McCarty were mediated by means other than the reduction in the number of polymorphs. These authors produced a leucopenia in dogs by using rabbit-anti-dog-polymorphonuclear serum. It was their conclusion that their findings were in accord with those of Phelps and McCarthy as regards the role of a vinblastine-induced leucopenia in preventing inflammation subsequent to the injection of mycrocrystalline urate into canine joints. Floresheim, et al. writing in Agents and Actions, 3 24 (1973) induced an acute arthritis in pigeons or chickens by the injection of microcrystalline sodium urate into the intertarsal joint. They found no inhibition of the arthritic response from a number of agents including both vinblastine and vincristine. Fitsgerald, et al., Pharmacology, 6, 265 (1971) used a different model--the sodium urate-induced paw swelling in mice. The authors found that various anti-mitotics including vinblastine and vincristine produced a significant depression of paw swelling at similar dose levels. The effects of the various anti-mitotic agents did not seem to bear any relation to their anti-mitotic potency. T. Y. Shen, in an article titled "The Expanding Vistas of Non-acidic Anti-arthritic Agents" in Drugs in Experimental Clinical Research Vol II (1) (1977) speculates that one approach, among many, for regulation of the immuno-pathology of arthritis would be to investigate the effect of selective membrane modulators upon this disease. According to Shen, "[p]hagocytosis and the function of membrane receptors and enzymes are subject to the regulation by the fluidity of the bi-layer membrane by the submembrane structures, microtubules and microfilaments . . . . " He reports that among the classical inhibitors of microtubules are included the vinca alkaloids, vinblastine and vincristine, the anti-tumor drug, maytensine, phodphyllotoxin and colchicin. Finally, in June, 1977, a question was raised as to whether it would be useful to use vinblastine in the treatment of systemic sclerosis (Abstracts of the 14th International Congress of Rheumatism--June 26, 1977, San Francisco, California--Abstract No. 661). The authors concluded that it would be. At the same meeting, a paper was presented (Abstract No. 426) concerning the effect of the intravenous administration of vinblastine on inflammation induced by the injection of pulverized calcium pyrophosphate dihydrate crystals into the pleural cavity. The authors concluded that vinblastine may have a suppressive effect on the inflammation thus induced.